These studies will characterize the alterations in muscle protein turnover seen in vitamin D deficiency. In paired feedings of vitamind D deficient rats and vitamin D supplemented controls, we plan to separate the direct effects of vitamin D deficiency from those of decreased caloric intake. Weight gain, muscle mass, muscle protein content, intracellular high energy phosphate and RNA levels will be determined. Individual and separate assessments of protein synthesis and degradation rates will be made using hemicorpus perfusion techniques. Protein synthesis will be assessed by the incorporation of (14C) phenylalanine into muscle. Muscle degradation will be determined by established methods, including the release of 3-methylhistidine from actinomyosin during myofibrillar degradation. We will also examine the extent of aggregation of ribosomal subunits. Actinomycin D will be used to determine whether vitamin D acts to increase DNA transcription of new messenger RNA, and vitamin D metabolites and synthetic analogs will be studied to determine which compounds are effective in altering protein turnover rates. Advances in our understanding of the actions of vitamin D within muscle could have important clinical relevance in conditions such as vitamin D dependent rickets, cirrhosis and chronic renal disease where vitamin D metabolism is known to be abnormal.